The mouse mammary tumor virus differs from most type-C systems in that the mature virions (B-particles) are produced in normal mammary gland throughout the animal's adult life. Current data suggests that the hormone regulation of MMTV expression is different in normal as compared to neoplastic mammary epithelium. This phenomenon is coincidental with increased MMTV DNA equivalents (copies) in neoplastic mammary epithelium. It is the object of this proposal to explore these phenomena in detail using nucleic acid hybridization in order to determine their biological significance. The integration of MMTV DNA into hormone independent sites in mammary epithelial DNA would be one working model of mouse mammary neoplasia. The appearance of uncontrolled MMTV expression could lead directly to unregulated growth. This and alternate hypotheses will be tested.